Chapter 18 Lecture 2024 - Cardiovascular System: The Heart PDF

Summary

These lecture notes from Chapter 18 cover the cardiovascular system, focusing on the heart. It includes discussions of heart structures, functions, layers and associated defects. This is not an exam paper; it is a lecture handout.

Full Transcript

The Cardiovascular System: The Heart Chapter 18 (18.1) The heart has four chambers and pumps blood through the pulmonary and systemic circuits Learning Objectives Describe the size, shape, location, and orientation of the heart in the thorax. Expl...

The Cardiovascular System: The Heart Chapter 18 (18.1) The heart has four chambers and pumps blood through the pulmonary and systemic circuits Learning Objectives Describe the size, shape, location, and orientation of the heart in the thorax. Explain how the structure of the three layers of the heart wall and pericardium are related to their functions Describe the structure and functions of the four heart chambers. The cardiovascular system includes the heart and blood vessels Heart Muscular pump Pushes blood into hollow vessels Chapter 18 Blood vessels Connected to heart Deliver blood to body tissues Chapter 19 The cardiovascular system constantly circulates blood Delivers to tissues Fresh nutrients Hormones Electrolytes Removes from tissues Metabolic wastes Nitrogenous wastes Carbon dioxide The heart is a double pump Right side of the heart is the “pulmonary pump” Pumps deoxygenated blood to lungs Left side of the heart is the “systemic pump” Pumps oxygenated blood to body Ventricular contraction ejects blood into pulmonary and systemic circuits Equal amount of blood goes to each Systemic circuit is much longer Has more resistance to blood flow Myocardium of left ventricle is thickest Must push harder to get its blood out The heart is in the mediastinum (thoracic cavity) Size of a fist Weighs less than 1 lb (hollow) 2/3 of mass lies left of body midline Broad base points toward right shoulder Narrow apex points towards left hip Apical impulse Tapping felt when heart contracts Caused when apex touches wall of chest Heart rotates forward during systole 5th intercostal space The pericardium Double walled sac that encloses the heart Two layers Fibrous pericardium Serous pericardium Fibrous pericardium Loose, superficial layer Tough Dense irregular connective tissue Functions Protect Anchor Prevent overfilling Dense Irregular connective tissue Serous pericardium Two layers forming a closed sac around heart Parietal layer (outer) Visceral layer (inner) AKA: epicardium Pericardial cavity Contains film of serous fluid Reduces friction Heart defect: pericarditis Inflammation of the pericardium Roughens serous membrane surfaces Heart rubs against pericardium as it beats Creaking sound in stethoscope Deep pain over sternum Heart defect: cardiac tamponade “heart plug” Caused by severe or prolonged pericarditis Large amount of fluid accumulates in pericardial cavity Heart is compressed Interferes with beating Treat with cardiocentesis Drain fluid with catheter The wall of the heart is made of 3 layers Epicardium Myocardium Endocardium Epicardium Most superficial Same as the visceral layer of the serous pericardium Infiltrated by fat with aging The myocardium Middle layer of heart wall Most of heart mass Thickness varies in different parts of the heart Made mostly of cardiac muscle cells Layer that contracts The endocardium Inner layer Lines chambers and valves Continuous with lining of blood vessels Glistening white, smooth endothelium Squamous epithelial cells on layer of connective tissue Reduces friction between blood and heart Think, Pair, Share We just discussed the layers of the heart wall and its coverings On your own (1 minute) List as many layers of the heart wall and coverings as you can remember and describe each layer's function if you can. With a neighbor (4 minuets) Compare your lists and put the layers in order from deepest to most superficial. Practice Questions True or False? Most of the heart is in the exact center of the thoracic cavity. Choose the pair that is not correctly matched. Myocardium – contracts Fibrous pericardium- reduces friction Pericardial cavity- reduces friction Endocardium- reduces friction Epicardium – same as visceral layer of serous pericardium Predict what would happen to the myocardium if the right side of the heart had to push against as much pressure as the left side does. (18.2) Heart valves make blood flow in one direction Learning Objective Explain the location, function, and mechanism of operation of the heart valves Make a rough sketch of heart anatomy Four valves keep blood flow unidirectional Thin flaps of connective tissue Closed valves block blood flow Open valves allow blood to pass through Atrioventricular (AV) valves Connect atria to ventricles Open when bp in atria > bp in ventricles Close when ventricles contract Prevents backflow into the atria The two AV valves Tricuspid valve Right AV valve Between right atrium and ventricle Three flaps Bicuspid valve Left AV valve Between left atrium and ventricle Two flaps AKA mitral valve Chordae tendineae (heart strings) Collagen cords connecting AV valves to ventricular wall At papillary muscle Ventricular contraction tugs on cords Holds valve flaps closed against high intraventricular pressure Semilunar (SL) valves Made of three flaps of tissue Located between ventricles and arteries Open when ventricles contract pressure in ventricles > pressure in arteries Close when ventricles relax Blood flows backward filling cusps The two SL valves Aortic SL valve (on left) Between aorta and left ventricle Pulmonary SL valve (on right) Between pulmonary trunk and right ventricle Work with a partner to brainstorm one similarity and two differences between the AV and SL valves Heart defect: incompetent valves Do not close all the way Leaky Causes backflow Heart re-pumps the same blood Danger of inadequate blood flow to tissues Diagnose by abnormal heart sounds More in lab Replacement of incompetent valves Mechanical valves Made from metal Last a long time Patient needs blood thinners Biosynthetic valves Made from treated tissue (won’t be rejected- antigens removed) Cadavers Pig valves Cow pericardium Heart defect: mitral valve prolapse Chordae tendineae don’t hold mitral valve in place during contraction It bulges into left atrium Can lead to… Incompetent valve Irregular heartbeat Pain Shortness of breath Fairly common Affects about 1% of population Found at 7% at autopsy (18.3) Blood flows from atrium to ventricle, and then to either the lungs or the rest of the body Learning Objectives Trace the pathway of blood through the heart. Describe the location and importance of the coronary arteries. Sketch the pathway of blood flow through the heart Coronary circulation The heart requires a large amount of fresh blood Without it cardiac tissue dies Coronary arteries supply the heart with blood Coronary arteries The main two leaving the aorta are Left coronary artery Right coronary artery Deliver blood when the heart is relaxed Squeezed shut by contraction of myocardium If blocked, oxygen is not delivered to myocardium Cardiac veins Collect blood and return it to heart Great, Middle, and Small Drain blood into coronary sinus Coronary sinus Drains directly into the right atrium Angina pectoris Thoracic pain Brief loss of blood to myocardium Causes Stress induces spasms of coronary arteries Physical activity Cardiac muscle cells weaken but do not die Myocardial infarction (MI) Heart attack Caused by prolonged coronary artery blockage Blood clots or plaque Cardiac muscle cells die If too much death, heart won’t beat If still alive dead cells replaced by connective tissue Dead cells fall apart releasing proteins that can be tested for CPK Troponin Think pair share… Make a list of the 6 cardiac defects we have learned about so far. (1 min on your own) Compare your list to a partner’s were there any missing? Which one do you think is the least life threatening? (4 min) (18.4) Intercalated discs connect cardiac muscle fibers into a functional syncytium Learning Outcome Compare and contrast the structural and functional properties of cardiac and skeletal muscle. Cardiac tissue has two cell types Cardiac muscle cells Actually contract Pacemaker cells Do not contract Located along conduction pathways Control timing of contraction Characteristics of cardiac muscle cells Short, fat, may be branched One or two nuclei Striated Sarcomeres of actin and myosin Electrically excitable Depolarization causes contraction Physically connected at intercalated discs Gap junctions Allow current to pass from cell to cell Desmosomes Keep tissue from tearing during contraction More Characteristics of cardiac muscle cells Contain over 10x more mitochondria than skeletal muscle Quickly die without oxygen Ischemia 1-3 hrs Longer absolute refractory period Time when cells cannot depolarize again Make a list... List all the characteristics of cardiac muscle cells you can remember (18.5) Pacemaker cells trigger action potentials thought the heart Learning Objectives Compare and contrast action potentials in cardiac pacemaker and contractile cells. Trace the conduction pathway through the heart Characteristics of pacemaker cells Do not contract Spontaneously produce action potentials Autorhythmic Located throughout heart along special conduction pathways More later Gap junctions spread the depolarizing current to cardiac muscle cells Causing contraction Pacemaker cells have unstable resting membrane potentials Hovers around -60 mV Due to closing of K+ channels and opening of slow Na+ channels Cell slowly becomes positive In most excitable cells resting membrane potential is constant K+ leak channels always open Threshold is -40 mV At -40 mV voltage-gated fast Ca2+ channels open Causes action potential Depolarizes to 0 mV Unique to pacemakers Usually Na+ influx causes action potential Triggers action potential in contractile cells Repolarization Voltage gated K+ channels open Same as in other muscle cells Draw an action potential for pacemaker cells. Indicate which ion channels are opening and closing. Conduction pathways run throughout the myocardium Made of pacemaker cells Connected to cardiac muscle cells by gap junctions Act as wires carrying the message to contract Sinoatrial (SA) node: initiates heartbeat Small mass of pacemaker cells in the right atrial wall Inferior to the superior vena cava Generates about 75 impulses per minute Faster than any other heart cell True pacemaker of the heart Where every beat begins Bachmann’s bundle: connects right and left atria Depolarization wave is quickly sent to left atrium Keeps atria in synch Depolarization of SA node causes both atria to contract at the same time No gap junctions between atrial and ventricular myocardium Ventricles do not contract Internodal pathways: connect SA to AV node Depolarization wave travels quickly to the atrioventricular (AV) node Located in the interatrial septum Near the tricuspid valve Atrioventricular (AV) node: delays depolarization Delays depolarization by 100 ms Smaller diameter Fewer gap junctions = bottleneck Enough time for atria to finish contraction before ventricles start Generates 50 impulses per minute Can run the heart if SA node is damaged Atrioventricular bundle: Connects AV node to ventricles AKA: bundle of His Only electrical connection between the atria and the ventricles Splits into the right and left bundle branches Bundles continue on to form Purkinje fibers Perkinje fibers: depolarize the contractile cells of the ventricles AKA subendocardial conducting network Also innervate papillary muscles Anchor chordae tendineae Ventricles contract from the apex Push blood superiorly b/c of anatomy of pathway 220 ms from SA node to systole Think, Pair, Share Name the indicated regions of the cardiac conduction network Which region depolarizes first? Which region depolarizes last? Which two regions depolarize at the same time? Depolarization of pacemaker cells causes depolarization of cardiac muscle cells because of gap junctions between cells Resting membrane potential is -90 mV in contractile cells Established by outward movement of K+ ions K+ leak channels are always open Similar to neurons and skeletal muscle Depolarization of contractile cells Voltage-gated fast Na+ channels open Faster than in skeletal muscle Na+ rapidly flows into cell Sarcolemma depolarizes to +30 mV How did the voltage-gates fast Na+ channels know to open? Depolarization triggers contraction At +30 mV Voltage-gated slow Ca2+ channels open Ca2+ enters the cell Causes contraction Plateau on graph Indicative of long absolute refractory period How does Ca2+ cause contraction? Repolarization of cardiac muscle cell Voltage-gated K+ channels open and K+ leaves the cell Membrane potential returns to - 90 mV Draw an action potential for contractile cardiac muscle cell. Indicate which ion channels are opening and closing. Absolute Refractory Period Time when cell cannot depolarize again Longer in cardiac muscle than skeletal muscle Prevents tetanic contractions Cramps, spasms, tremors Ion imbalances Hypercalcemia Too much calcium Causes prolonged and spastic heart contractions Ion imbalances: Hypocalcemia Low calcium levels Reduces the force of each heartbeat Ion imbalances: Hyperkalemia High potassium levels Speeds up membrane repolarization disrupting heart rhythm Ion imbalances: Hypernatremia Blood Na+ concentration is too high Prevents the entry of calcium into the myocardium Heart beats feebly Heart defect: arrhythmia Uncoordinated atrial and ventricular contraction Often the ventricles contract too soon Do not properly fill with blood Types of arrhythmia Paroxysmal atrial tachycardia (PAT) Burst of atrial contractions Ventricular tachycardia (V-tac) Rapid, uncoordinated ventricular contractions Heart defect: fibrillation Rapid and irregular contraction of cardiac muscle Tachycardia can lead to fibrillation A defibrillator can be used to depolarize the heart Restarts entire electrical system Heart defect: ectopic focus Inappropriate region of the heart controls rhythm Can appear in atria or ventricles Caused by… Ischemic damage to conduction pathways Stimulants Fever Can lead to arrhythmias and fibrillation Heart defect: heart block Damage to AV node or AV bundle Drugs or disease First degree Depolarization is delayed for too long Second degree Only some of the impulses are transmitted Third degree No action potentials pass to the ventricles AKA: complete heart block Heart defect: asystole Period when heart fails to contract Neither atria nor ventricles contract No electrical signals from cardiac muscle Flatline Practice Questions True or False? All cardiac muscle has an unstable resting membrane potential. Which ion is most directly responsible for depolarization in pacemaker cells? Na+ Ca2+ Cl- K+ Describe as many similarities and differences as you can between cardiac and skeletal muscle. (18.6) The cardiac cycle describes the mechanical events associated with blood flow through the heart Learning Objective Describe the timing and events of the cardiac cycle The cardiac cycle Systole All the events associated with blood flow through the heart in one heart beat Terminology Systole = contract Contractions leads to pressure changes that open valves and move blood If no valves are open volume in chambers doesn’t change = Diastole isovolumetric Diastole = relax Atria and ventricles contract and relax at different times during cardiac cycle Assume we are referring to ventricles unless atrial is stated Use hands to simulate contractions during cardiac cycle Early-Mid Diastole All chambers relaxed Late Diastole Atria contract Ventricles still relaxed Systole Atria relax Ventricles contract Overview of steps 1. Ventricular filling Mid-to-late diastole 2. Isovolumetric contraction First part of systole 3. Ventricular ejection Most of systole 4. Isovolumetric relaxation Early diastole Step 1: Ventricular Filling Occurs from mid-to-late diastole Begins when atria and ventricles are completely relaxed Pressure in ventricles is low SL valves are closed AV valves are open 80% of blood passively flows into ventricles Ends with atrial contraction Remaining 20% of blood forced into ventricles Step 2: Isovolumetric Contraction Occurs at beginning of systole Atria relax and ventricles begin contracting Pressure in ventricles starts increasing AV valves go from open to closed All valves closed for a split second Ventricles are at fullest point EDV (End Diastolic Volume) Step 3: Ventricular ejection Occurs during most of systole Blood is leaving the heart through the great arteries SL valves open when ventricular pressure > pressure in great arteries (afterload) AV valves still closed Step 4: Isovolumetric relaxation Occurs at early diastole SL valves go from open to closed Caused by pressure decreasing as ventricles relax When aortic SL valves close pressure in aorta spikes Dicrotic notch AV valves still closed Ventricles are at their emptiest ESV (End Systolic Volume) Sketch the cardiac cycle in 5 hearts Pressure Changes During the Cardiac Cycle Blue line = pressure in left ventricle Purple line = pressure in left atrium D Green line = pressure in aorta C At “A” on the graph the AV valves are open because the pressure in the atrium is higher than the pressure in the ventricle. 1. Follow the blue line. At first the pressure in the ventricle (blue) is lower than the pressure in the atrium (purple), but then it B E changes. What is causing the pressure in A the ventricles to increase and then decrease again? 2. For each circled point decide if the AV and SL valves are open or closed. Practice Questions True or False? During ventricular ejection, the atria are relaxed. Which valves go from closed to open at the end of isovolumetric relaxation? AV SL Both Neither How many times during a single cardiac cycle are all four valves closed? (18.7) Stroke volume and heart rate are Regulated to alter cardiac output Learning Objectives Predict the effects of various factors regulating stroke volume and heart rate. Stroke Volume (SV) The total amount of blood ejected from one ventricle in one cardiac cycle EDV-ESV=SV Remember equal amounts of blood leave right and left ventricles Pressure values are different Three variables regulate stroke volume Preload Afterload Contractility Preload: degree of stretch of cardiac muscle More stretch = larger EDV Larger EDV = larger SV Frank-Starling law: Heart will pump any amount of blood delivered to it in a single stroke Increasing venous return increases preload Exercise Afterload: back pressure from arterial blood vessels Vascular resistance to cardiac emptying during systole Must be overcome to force blood out of heart If a person has high diastolic bp Heart must contract with a greater force to pump the same amount of blood Heart works harder Contractility: force of contraction A measure of how much force is generated by each cardiac cell Inotropic effectors change contractility Positive inotropic effectors Increase force Negative inotropic effectors Decrease force Think, Pair, Share We just discussed three factors that can affect stroke volume. On your own (1 minute) Predict what effect increase preload, afterload, and contractility will have on stroke volume With a neighbor (2 minuets) Compare your predictions Positive inotropic effectors Activation of sympathetic nervous system Glucagon TH Epinephrine/NE Digitalis Given when heart not pumping enough blood Congestive heart failure Negative inotropic effectors Acidosis Excess H+ High extracellular K+ Calcium channel blockers Decreases time of contraction Heart rate is how often the heart contracts Average is about 75 beats per minute When did we see this number before? Chronotropic effectors change the speed of the heart Positive or Negative Positive chronotropic factors increase heart rate Activation of the sympathetic nervous system Epinephrine Norepinephrine T3/T4 (TH) Heat Tachycardia (hurry heart) Abnormally fast heartbeat Greater than 100 bpm Caused by Fever Stress Drugs Heart disease Can lead to fibrillation Negative chronotropic factors decrease heart rate Activation of the parasympathetic nervous system Via vagus nerve Cold Bradycardia Abnormally slow heart rate Less than 60 bmp Caused by Hypothermia Drugs Heroin THC Parasympathetic NS activation Cardiac output (CO) The amount of blood pumped out by each ventricle in 1 minute Cardiac output = heart rate x stroke volume CO = HR x SV Heart defect: heart palpitations Increased force of contraction causes a noticeable heartbeat Most are not life threatening Symptomatic of mild arrhythmias Heart defect: congestive heart failure Weak or damaged myocardium Heart cannot maintain adequate blood flow Causes Multiple myocardial infarctions Hypertension Coronary atherosclerosis Two types Pulmonary Peripheral Pulmonary Congestion Left side of heart fails Right side still pumping away into lungs Blood is trapped in pulmonary circuit Causes pulmonary edema Interferes with gas exchange in lungs Peripheral congestion (Cor pulmonale) Right side of heart fails Blood accumulates in systemic circulation Caused by high bp in pulmonary arteries Acute cases due to embolism Chronic cases due to lung damage Usually caused by smoking Heart defect: fibrosis Dead contractile cells are replaced with non-contractile scar tissue Interferes with Contraction Electrical conduction Practice Questions True or False? Taking digitalis should increase cardiac output. Which of the following increases afterload? Exercise High blood pressure in the aorta Cold Heat Explain why failure of the right side of the heart causes peripheral congestion.

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